Journal articles: 'Structure of histamines'

1

Sukamoto, Takayuki, and Tadayuki Saito. "The structure-activity relationship of anti-histamines." Japanese Journal of Pharmacology 71 (1996): 18. http://dx.doi.org/10.1016/s0021-5198(19)36336-x.

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Dave, Shikha S., and Anjali M. Rahatgaonkar. "Computational Evaluation of 2-Phenyl-4H-chromen-4-one Analogues as Antihistamines: Potential HistamineN-Methyltransferase (HMT) Inhibitors." E-Journal of Chemistry 6, no. 4 (2009): 1009–16. http://dx.doi.org/10.1155/2009/497124.

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Abnormal release of histamine, which is present in relatively high concentration in the lungs, causes serious allergic vasoconstriction and anaphylactic manifestation in human beings. In mammals, a major pathway of histamine metabolism in the lungs is mediated by histamineN-methyl transferase (HMT) and diamine oxidase. The need to design a strategy of mechanistic computational evaluation of protein-ligand affinityi.e. HMT- 2-phenyl-4H-chromen-4-ones, protein complex binding energy has been established. A library of synthesized 2-phenyl-4H-chromen-4-ones was docked into the active site cavity of target protein, HMT (Pdb: 2aot). The high-resolution crystal structure of HMT complex with the competitive inhibitorN[2 (benzhydryloxy)ethyl]N N-Dimethylamine (Diphenhydramine) revealed a protein with a highly confined binding region that could be targeted in the design of specific anti-histamines. The validation of docking programme by Potential Mean Force was compared with binding energy results of known ligands in the active sites of HMT, diphenhydramine / benadryl, promethazine, cyproheptadine, trimeton / aviletc. All the synthesized chromone derivatives showed comparable negative binding energies pointing towards the fact that these molecules could be potent antihistamines.

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Kubota, Katsumi, Hirotaka Kurebayashi, Hirotaka Miyachi, Masanori Tobe, Masako Onishi, and Yoshiaki Isobe. "Synthesis and structure–activity relationship of tricyclic carboxylic acids as novel anti-histamines." Bioorganic & Medicinal Chemistry 19, no. 9 (May 2011): 3005–21. http://dx.doi.org/10.1016/j.bmc.2011.03.003.

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Kljun, Jakob, Saša Petriček, Dušan Žigon, Rosana Hudej, Damijan Miklavčič, and Iztok Turel. "Synthesis and Characterization of Novel Ruthenium(III) Complexes with Histamine." Bioinorganic Chemistry and Applications 2010 (2010): 1–6. http://dx.doi.org/10.1155/2010/183097.

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Novel ruthenium(III) complexes with histamine[RuCl4(dmso-S)(histamineH)]⋅O(1a) and[RuCl4(dmso-S)(histamineH)](1b) have been prepared and characterized by X-ray structure analysis. Their crystal structures are similar and show a protonated amino group on the side chain of the ligand which is not very common for a simple heterocyclic derivative such as histamine. Biological assays to test the cytotoxicity of the compound1bcombined with electroporation were performed to determine its potential for future medical applications in cancer treatment.

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Wang, Wentao, Fadi Aldeek, Xin Ji, Birong Zeng, and Hedi Mattoussi. "A multifunctional amphiphilic polymer as a platform for surface-functionalizing metallic and other inorganic nanostructures." Faraday Discuss. 175 (2014): 137–51. http://dx.doi.org/10.1039/c4fd00154k.

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We designed a new set of polymer ligands that combine multiple metal-coordinating groups and short polyethylene glycol (PEG) moieties in the same structure. The ligand design relies on the controlled grafting of a large number of amine-terminated histamines and PEG short chains onto a poly(isobutylene-alt-maleic anhydride) backbone,viaa one-step nucleophilic addition reaction. This addition reaction is highly efficient, can be carried out in organic media and does not require additional reagents. We show that when imidazole groups are used the resulting polymer ligand can strongly ligate onto metal nanostructures such as nanoparticles (NPs) and nanorods (NRs) made of gold cores. The resulting polymer-coated NPs and NRs exhibit good colloidal stability to pH changes and added electrolytes. This constitutes a departure from the use of thiol-based ligands to coordinate on Au surfaces. The present chemical approach also opens up additional opportunities for designing hydrophilic and reactive platforms where the polymer coating can be adjusted to various metal and metal oxide surfaces by simply modifying or combining the addition reaction with other metal coordinating groups. These could include iron oxide NPs and semiconductor QDs. These polymer-capped NPs and NRs can be used to develop biologically-active platforms with potential use for drug delivery and sensing.

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6

Suki, B., Q. Zhang, and K. R. Lutchen. "Relationship between frequency and amplitude dependence in the lung: a nonlinear block-structured modeling approach." Journal of Applied Physiology 79, no. 2 (August 1, 1995): 660–71. http://dx.doi.org/10.1152/jappl.1995.79.2.660.

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During lung constriction, there is an increase in both the frequency and tidal volume (VT) dependences of lung tissue resistance (Rti) and elastance (Eti). This suggests that 1) significant alterations take place in the mechanisms contributing to both the linear and nonlinear characteristics of lung tissues; and 2) the frequency and VT dependences of Rti and Eti are coupled. We examined these issues for the case of sine wave and special pseudorandom inputs by utilizing the theory of nonlinear block-structured systems. Two basic model structures were considered: the Hammerstein and the Wiener structures. The Hammerstein structure is a cascade connection of a nonlinear zero-memory (N) system and a linear dynamic process (L). This structure predicts that frequency and VT dependences of Rti and Eti are decoupled. The Wiener structure is an inverse cascade of these two blocks (i.e., L-N) in which the frequency and VT dependences of Rti and Eti are coupled. These two structures were combined with a nonlinear airway compartment and fitted to measured airway opening and alveolar capsule pressure-flow time domain data in dogs before and after histamine-induced constriction. The best lung model was a linear airway compartment combined with a Wiener structure consisting of a constant-phase linear tissue impedance in cascade with a polynomial nonlinearity, suggesting that frequency and VT dependences of Rti and Eti are indeed coupled during control and constricted conditions. Moreover, histamine caused much larger changes in the linear tissue parameters than in the nonlinear coefficients.

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7

Rangachari, P. K., T. Prior, R. A. Bell, and T. Huynh. "Histamine potentiation by hydroxylamines: structure-activity relations; inhibition of diamine oxidase." American Journal of Physiology-Gastrointestinal and Liver Physiology 263, no. 5 (November 1, 1992): G632—G641. http://dx.doi.org/10.1152/ajpgi.1992.263.5.g632.

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Hydroxylamines potentiated the responses of the canine colonic epithelium to histamine but not to other agonists such as serotonin or carbachol. We tested the hypothesis that an inhibition of histamine catabolism could explain the observed potentiation. A clear structure activity relation was defined, active compounds having the structure NH2-O-R, R being a simple uncharged aliphatic group. Active compounds delayed the disappearance of histamine from the bathing solutions and inhibited colonic diamine oxidase, an effect mimicked by standard inhibitors aminoguanidine and semicarbazide. Histamine agonists that possessed an imidazole nucleus (2- and 4-methylhistamine) were affected, whereas impromidine, 2 pyridylethylamine, and dimaprit were not. Agonist specificity combined with the enzyme data suggest an inhibition of histamine catabolism as a possible mechanism for the potentiating effects observed.

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8

Cole, L. B., and E. M. Holt. "Structure of (histamine.2H+)(ZnCl4)." Acta Crystallographica Section C Crystal Structure Communications 46, no. 9 (September 15, 1990): 1737–39. http://dx.doi.org/10.1107/s0108270190002773.

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9

Jin, Cong-Yu, Hong Wei, Kaj Karlstedt, and Antti Pertovaara. "Histamine in the locus coeruleus attenuates neuropathic hypersensitivity." Scandinavian Journal of Pain 4, no. 4 (October 1, 2013): 259–60. http://dx.doi.org/10.1016/j.sjpain.2013.07.015.

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AbstractAimsAmong brain structures receiving efferent projections from the histaminergic tuberomammillary nucleus is the pontine locus coeruleus (LC), a structure involved in descending noradrenergic control of pain. Here we studied whether histamine in the LC is involved in descending regulation of neuropathic hypersensitivity.MethodsPeripheral neuropathy was induced by unilateral spinal nerve ligation (SNL) in the rat with a chronic intracerebral and intrathecal catheter for drug administrations. Mechanical hypersensitivity in the injured limb was assessed by monofilaments. Heat nociception was assessed by determining radiant heat-induced paw flick.ResultsHistamine in the LC (ipsilateral to nerve injury) produced a dose-related (1–10 μg) mechanical antihypersensitivity effect (maximum effect at 15 min and duration of effect 30 min), without influence on heat nociception. Pretreatment of LC with zolantidine (H2 receptor antagonist), but not with pyrilamine (H1 receptor antagonist), reversed the antihypersensitivity effect of histamine. Zolantidine or pyrilamine alone in LC failed to influence pain behavior. The antihypersensitivity effect induced by histamine in LC was reduced also by spinal administration of atipamezole (an α2-adrenoceptor antagonist).ConclusionsThe results indicate that histamine acting on H2 receptors in the LC attenuates mechanical hypersensitivity in peripheral neuropathy. The histamine-induced descending antihypersensitivity effect is at least partly mediated by noradrenergic pathways acting on the spinal α2-adrenoceptor.

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10

Tikhonov, Denis S., Anatolii N. Rykov, Olga E. Grikina, and Leonid S. Khaikin. "Gas phase equilibrium structure of histamine." Physical Chemistry Chemical Physics 18, no. 8 (2016): 6092–102. http://dx.doi.org/10.1039/c5cp07719b.

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11

Yamauchi, K., K. Sekizawa, H. Suzuki, H. Nakazawa, Y. Ohkawara, D. Katayose, H. Ohtsu, et al. "Structure and function of human histamine N-methyltransferase: critical enzyme in histamine metabolism in airway." American Journal of Physiology-Lung Cellular and Molecular Physiology 267, no. 3 (September 1, 1994): L342—L349. http://dx.doi.org/10.1152/ajplung.1994.267.3.l342.

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In mammals, histamine is inactivated principally by two enzymes: histamine N-methyltransferase (HMT; EC 2.1.1.8) and diamine oxidase (DAO; EC 1.4.3.6.). The cDNA clone of human HMT (hHMT) has been isolated from a cDNA library of human kidney and its nucleotide, and deduced amino acid sequences have been determined. One clone, phHMT-1, containing an insert of 1.4 kb, was confirmed to encode HMT by transient expression of HMT activity in COS cells. hHMT consists of 292 amino acid residues [relative molecular weight (M(r)) = 33,279] and shares 82% identity with that of rat HMT. Northern blot analysis with hHMT cDNA probe revealed that 1.6-kb HMT mRNA transcript was expressed in the lung, nasal polyps, and kidney. HMT activity was measured in human trachea and bronchi. In addition, the contractile response of isolated human bronchi to histamine was potentiated in the presence of an HMT inhibitor, SKF 91488, but a DAO inhibitor, aminoguanidine, was without effect. These results suggest that HMT plays an important role in degrading histamine and in regulating the airway response to histamine. Therefore, the level of HMT gene expression in human airway may be one of the critical factors determining the airway responsiveness to histamine. In situ chromosomal hybridization demonstrated that human HMT gene was localized in chromosome 1 p32.

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12

Benetti, Fernando, Cristiane Regina Guerino Furini, Jociane de Carvalho Myskiw, Gustavo Provensi, Maria Beatrice Passani, Elisabetta Baldi, Corrado Bucherelli, Leonardo Munari, Ivan Izquierdo, and Patrizio Blandina. "Histamine in the basolateral amygdala promotes inhibitory avoidance learning independently of hippocampus." Proceedings of the National Academy of Sciences 112, no. 19 (April 27, 2015): E2536—E2542. http://dx.doi.org/10.1073/pnas.1506109112.

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Recent discoveries demonstrated that recruitment of alternative brain circuits permits compensation of memory impairments following damage to brain regions specialized in integrating and/or storing specific memories, including both dorsal hippocampus and basolateral amygdala (BLA). Here, we first report that the integrity of the brain histaminergic system is necessary for long-term, but not for short-term memory of step-down inhibitory avoidance (IA). Second, we found that phosphorylation of cyclic adenosine monophosphate (cAMP) responsive-element-binding protein, a crucial mediator in long-term memory formation, correlated anatomically and temporally with histamine-induced memory retrieval, showing the active involvement of histamine function in CA1 and BLA in different phases of memory consolidation. Third, we found that exogenous application of histamine in either hippocampal CA1 or BLA of brain histamine-depleted rats, hence amnesic, restored long-term memory; however, the time frame of memory rescue was different for the two brain structures, short lived (immediately posttraining) for BLA, long lasting (up to 6 h) for the CA1. Moreover, long-term memory was formed immediately after training restoring of histamine transmission only in the BLA. These findings reveal the essential role of histaminergic neurotransmission to provide the brain with the plasticity necessary to ensure memorization of emotionally salient events, through recruitment of alternative circuits. Hence, our findings indicate that the histaminergic system comprises parallel, coordinated pathways that provide compensatory plasticity when one brain structure is compromised.

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13

Söderberg, M., R. Lundgren, S. Hellström, P. Hörstedt, and A. Bergh. "Bronchial mucosal structure after histamine inhalation." Allergy 48, no. 1 (January 1993): 25–29. http://dx.doi.org/10.1111/j.1398-9995.1993.tb02171.x.

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14

DE BACKER, Marianne D., Inge LOONEN, Peter VERHASSELT, Jean-Marc NEEFS, and Walter H. M. L. LUYTEN. "Structure of the human histamine H1 receptor gene." Biochemical Journal 335, no. 3 (November 1, 1998): 663–70. http://dx.doi.org/10.1042/bj3350663.

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Histamine H1 receptor expression has been reported to change in disorders such as allergic rhinitis, autoimmune myocarditis, rheumatoid arthritis and atherosclerosis. Here we report the isolation and characterization of genomic clones containing the 5´ flanking (regulatory) region of the human histamine H1 receptor gene. An intron of approx. 5.8 kb was identified in the 5´ untranslated region, which suggests that an entire subfamily of G-protein-coupled receptors may contain an intron immediately upstream of the start codon. The transcription initiation site was mapped by 5´ rapid amplification of cDNA ends to a region 6.2 kb upstream of the start codon. Immediately upstream of the transcription start site a fragment of 1.85 kb was identified that showed promoter activity when placed upstream of a luciferase reporter gene and transiently transfected into cells expressing the histamine H1 receptor. The promoter sequence shares a number of characteristics with the promoter sequences of other G-protein-coupled receptor encoding genes, including binding sites for several transcription factors, and the absence of TATA and CAAT sequences at the appropriate locations. The promoter sequence described here differs from that reported previously [Fukui, Fujimoto, Mizuguchi, Sakamoto, Horio, Takai, Yamada and Ito (1994) Biochem. Biophys. Res. Commun. 201, 894–901] because the reported genomic clone was chimaeric. Furthermore our study provides evidence that the 3´ untranslated region of the H1 receptor mRNA is much longer than previously accepted. Together, these findings provide a complete view of the structure of the human histamine H1 receptor gene. Both the coding region of the H1 receptor gene and its promoter region were independently mapped to chromosome 3p25.

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15

Adimi, Maryam, Mahmoud Salimi, and Mehdi Nekoei. "QSAR study on the histamine (H3) receptor antagonists using the genetic algorithm: Multi parameter linear regression." Journal of the Serbian Chemical Society 77, no. 5 (2012): 639–50. http://dx.doi.org/10.2298/jsc110804205a.

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A quantitative structure activity relationship (QSAR) model has been produced for predicting antagonist potency of biphenyl derivatives as human histamine (H3) receptors. The molecular structures of the compounds are numerically represented by various kinds of molecular descriptors. The whole data set was divided into training and test sets. Genetic algorithm based multiple linear regression is used to select most statistically effective descriptors. The final QSAR model (N =24, R2=0.916, F = 51.771, Q2 LOO = 0.872, Q2 LGO = 0.847, Q2 BOOT = 0.857) was fully validated employing leaveone- out (LOO) cross-validation approach, Fischer statistics (F), Yrandomisation test, and predictions based on the test data set. The test set presented an external prediction power of R2 test=0.855. In conclusion, the QSAR model generated can be used as a valuable tool for designing similar groups of new antagonists of histamine (H3) receptors.

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16

Knigge, Ulrich, Steen Matzen, and Jørgen Warberg. "Effects of H2-receptor antagonists on prolactin secretion: Specificity and mediation of the response." Acta Endocrinologica 115, no. 4 (August 1987): 461–68. http://dx.doi.org/10.1530/acta.0.1150461.

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Abstract. The effects on prolactin secretion of histamine H2-receptor antagonists infused intracerebroventricularly were studied in urethane anaesthetized male rats. A dose of 1.6 μmol cimetidine stimulated basal prolactin secretion and did not affect the histamine-induced release, whereas 0.4 μmol cimetidine inhibited basal and histamine-stimulated prolactin secretion. 0.1 μmol cimetidine had no effect. The more potent H2-receptor antagonist ranitidine at doses of 0.1, 0.4, 1.6 μmol had no effect on basal prolactin secretion, whereas 0.4 and 1.6 μmol inhibited the histamine-stimulated secretion completely. SKF-92408, a compound resembling cimetidine in chemical structure but devoid of H2-receptor antagonist activity, stimulated basal prolactin secretion at a dose of 1.6 μmol, but had no effect on the histamine-induced release or at a dose of 0.4 μmol. The H2-receptor antagonists metiamide and oxmetidine (1.6 μmol) stimulated basal prolactin secretion and did not prevent the response to histamine. A dose of 0.4 or 1.6 μmol imidazole (the ring structure contained in cimetidine, SKF-92408, metiamide, and oxmetidine) had no effect on basal or histamine-stimulated prolactin secretion. The findings indicate that cimetidine stimulates prolactin secretion by a non-specific action when infused centrally at high doses. In contrast, when infused at lower doses cimetidine inhibits the basal and histamine-stimulated secretion by blockade of H2-receptors. The prolactin-stimulatory action of cimetidine was not due to an H2-agonist effect, since ranitidine did not prevent the response. Cimetidine did not stimulate prolactin secretion via an effect on the dopaminergic system, since the drug had no effect on the dopamine concentration in hypophysial portal blood or in hypothalamic tissue and since inhibition of the dopamine synthesis by α-methyl-p-tyrosine did not prevent the cimetidine-induced prolactin release.

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17

Shimamura, Tatsuro. "X-ray structure of histamine H1 receptor." Folia Pharmacologica Japonica 144, no. 1 (2014): 43–44. http://dx.doi.org/10.1254/fpj.144.43.

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18

Reed, Timothy, Gerald H. Lushington, Yan Xia, Hidehiko Hirakawa, DeAnna M. Travis, Minae Mure, Emily E. Scott, and Julian Limburg. "Crystal Structure of Histamine Dehydrogenase fromNocardioides simplex." Journal of Biological Chemistry 285, no. 33 (June 10, 2010): 25782–91. http://dx.doi.org/10.1074/jbc.m109.084301.

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19

Stamato, Fulvia M. L. G., Marco A. Perez, and Elson Longo. "Structure-activity relationships for histamine H2-antagonists." Journal of Molecular Structure: THEOCHEM 210 (November 1990): 447–53. http://dx.doi.org/10.1016/0166-1280(90)80068-y.

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20

Chen, Duan, Takeshi Aihara, Chun-Mei Zhao, Rolf Håkanson, and Susumu Okabe. "Differentiation of the Gastric Mucosa I. Role of histamine in control of function and integrity of oxyntic mucosa: understanding gastric physiology through disruption of targeted genes." American Journal of Physiology-Gastrointestinal and Liver Physiology 291, no. 4 (October 2006): G539—G544. http://dx.doi.org/10.1152/ajpgi.00178.2006.

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Many physiological functions of the stomach depend on an intact mucosal integrity; function reflects structure and vice versa. Histamine in the stomach is synthesized by histidine decarboxylase (HDC), stored in enterochromaffin-like (ECL) cells, and released in response to gastrin, acting on CCK2 receptors on the ECL cells. Mobilized ECL cell histamine stimulates histamine H2 receptors on the parietal cells, resulting in acid secretion. The parietal cells express H2, M3, and CCK2 receptors and somatostatin sst2 receptors. This review discusses the consequences of disrupting genes that are important for ECL cell histamine release and synthesis (HDC, gastrin, and CCK2 receptor genes) and genes that are important for “cross-talk” between H2 receptors and other receptors on the parietal cell (CCK2, M3, and sst2 receptors). Such analysis may provide insight into the functional significance of gastric histamine.

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21

Dvorak, AM, DW Jr MacGlashan, ES Morgan, and LM Lichtenstein. "Histamine distribution in human basophil secretory granules undergoing FMLP-stimulated secretion and recovery." Blood 86, no. 9 (November 1, 1995): 3560–66. http://dx.doi.org/10.1182/blood.v86.9.3560.bloodjournal8693560.

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We examined subcellular histamine localizations in purified human basophils that were stimulated to degranulate with FMLP using an ultrastructural enzyme-affinity technique. Basophils were collected at early (0, 20 seconds, 1 minute) and late (10 minutes to 6 hours) time points poststimulation and were prepared for routine ultrastructural and diamine oxidase-gold (DAO-gold) cytochemical analysis. Histamine was present in unaltered cytoplasmic secretory granules (30.77 gold particles per square micrometer; P < .001 compared with background); specificity controls (histamine absorption, diamine oxidase digestion) abrogated granule labeling for histamine. Altered granules in stimulated cells were not significantly labeled for histamine, as compared with background (P = not significant); unaltered granules in the same cells contained more histamine than altered granules (P < .05). During recovery times, spanning 10 minutes to 6 hours, granules again appeared to be electron-dense and contained histamine (33.49/microns2; P = not significant as compared with unaltered granules in 1-minute FMLP-stimulated cells, and P < .05 as compared with altered granules in 1-minute FMLP-stimulated samples). Other structures devoid of histamine in actively secreting cells included extruded granules and intragranular and extruded Charcot-Leyden crystals. Recovering basophils displayed morphologic evidence of material and membrane conservation, granule content condensation, and biosynthesis. Subcellular histamine-rich sites in actively recovering basophils included condensing granules and collections of cytoplasmic vesicles in three locations: beneath the plasma membrane, adjacent to granules, and in the Golgi region. These studies show that unaltered granules of actively releasing human basophils, as well as similar granules that are reconstituted after FMLP-stimulated degranulation, contain histamine, but that altered granules in stimulated cells undergoing degranulation are devoid of histamine. Reconstitution of histamine-rich granules is associated with DAO-gold-positive cytoplasmic vesicles, suggesting transport of histamine derived from either new synthesis, re-uptake of released histamine, or both, to reconstituted granules.

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Pertz, Heinz, Sigurd Elz, and Walter Schunack. "Structure-Activity Relationships of Histamine H1-Receptor Agonists." Mini-Reviews in Medicinal Chemistry 4, no. 9 (November 1, 2004): 935–40. http://dx.doi.org/10.2174/1389557043403198.

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23

Dove, Stefan, Sigurd Elz, Roland Seifert, and Armin Buschauer. "Structure-Activity Relationships of Histamine H2 Receptor Ligands+." Mini-Reviews in Medicinal Chemistry 4, no. 9 (November 1, 2004): 941–54. http://dx.doi.org/10.2174/1389557043403242.

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24

Weyand, S., T. Shimamura, M. Shiroshi, H. Tsujimoto, G. Winter, V. Katritch, R. Abagyan, et al. "The structure of the human histamine H1 receptor." Acta Crystallographica Section A Foundations of Crystallography 68, a1 (August 7, 2012): s29. http://dx.doi.org/10.1107/s0108767312099448.

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Nieto-Alamilla, Gustavo, Ricardo Márquez-Gómez, Ana-Maricela García-Gálvez, Guadalupe-Elide Morales-Figueroa, and José-Antonio Arias-Montaño. "The Histamine H3 Receptor: Structure, Pharmacology, and Function." Molecular Pharmacology 90, no. 5 (August 25, 2016): 649–73. http://dx.doi.org/10.1124/mol.116.104752.

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26

Wojtczak, A., Z. Kosturkiewicz, and A. Surdykowski. "Structure of carbonatobis(histamine)cobalt(III) chloride monohydrate." Acta Crystallographica Section C Crystal Structure Communications 46, no. 4 (April 15, 1990): 578–81. http://dx.doi.org/10.1107/s0108270189007766.

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Juang, Yu-Chi, Xavier Fradera, Yongxin Han, and Anthony William Partridge. "Repurposing a Histamine Detection Platform for High-Throughput Screening of Histidine Decarboxylase." SLAS DISCOVERY: Advancing the Science of Drug Discovery 23, no. 9 (June 8, 2018): 974–81. http://dx.doi.org/10.1177/2472555218778053.

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Histidine decarboxylase (HDC) is the primary enzyme that catalyzes the conversion of histidine to histamine. HDC contributes to many physiological responses as histamine plays important roles in allergic reaction, neurological response, gastric acid secretion, and cell proliferation and differentiation. Small-molecule modulation of HDC represents a potential therapeutic strategy for a range of histamine-associated diseases, including inflammatory disease, neurological disorders, gastric ulcers, and select cancers. High-throughput screening (HTS) methods for measuring HDC activity are currently limited. Here, we report the development of a time-resolved fluorescence resonance energy transfer (TR-FRET) assay for monitoring HDC activity. The assay is based on competition between HDC-generated histamine and fluorophore-labeled histamine for binding to a Europium cryptate (EuK)-labeled anti-histamine antibody. We demonstrated that the assay is highly sensitive and simple to develop. Assay validation experiments were performed using low-volume 384-well plates and resulted in good statistical parameters. A pilot HTS screen gave a Z′ score > 0.5 and a hit rate of 1.1%, and led to the identification of a validated hit series. Overall, the presented assay should facilitate the discovery of therapeutic HDC inhibitors by acting as a novel tool suitable for large-scale HTS and subsequent interrogation of compound structure–activity relationships.

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Komori, Hirofumi, Yoko Nitta, Hiroshi Ueno, and Yoshiki Higuchi. "Structural basis for the histamine synthesis by human histidine decarboxylase." Acta Crystallographica Section A Foundations and Advances 70, a1 (August 5, 2014): C458. http://dx.doi.org/10.1107/s2053273314095412.

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Histamine is a bioactive amine responsible for a variety of physiological reactions, including allergy, gastric acid secretion, and neurotransmission. In mammals, histamine production from histidine is catalyzed by histidine decarboxylase (HDC). Mammalian HDC is a pyridoxal 5'-phosphate (PLP)-dependent decarboxylase and belongs to the same family as mammalian glutamate decarboxylase (GAD) and mammalian aromatic L-amino acid decarboxylase (AroDC). The decarboxylases of this family function as homodimers and catalyze the formation of physiologically important amines like GABA and dopamine via decarboxylation of glutamate and DOPA, respectively. Despite high sequence homology, both AroDC and HDC react with different substrates. For example, AroDC catalyzes the decarboxylation of several aromatic L-amino acids, but has little activity on histidine. Although such differences are known, the substrate specificity of HDC has not been extensively studied because of the low levels of HDC in the body and the instability of recombinant HDC, even in a well-purified form. However, knowledge about the substrate specificity and decarboxylation mechanism of HDC is valuable from the viewpoint of drug development, as it could help lead to designing of novel drugs to prevent histamine biosynthesis. We have determined the crystal structure of human HDC in complex with inhibitors, histidine methyl ester (HME) and alpha-fluoromethyl histidine (FMH). These structures showed the detailed features of the PLP-inhibitor adduct (external aldimine) in the active site of HDC. These data provided insight into the molecular basis for substrate recognition among the PLP-dependent L-amino acid decarboxylases.

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Salachas, F., E. Schneider, FM Lemoine, B. Lebel, M. Daeron, S. Navarro, H. Ziltener, and M. Dy. "Aggregated IgE mimic interleukin-3-induced histamine synthesis by murine hematopoietic progenitors." Blood 84, no. 4 (August 15, 1994): 1098–107. http://dx.doi.org/10.1182/blood.v84.4.1098.1098.

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Abstract Similar to interleukin-3 (IL-3), IgE acts on murine bone marrow cells by inducing histamine production. This effect does not result from degranulation of histamine-containing cells, but from histamine synthesis, as assessed by the following findings. (1) The histamine content of freshly isolated bone marrow cells is too low to account for the increase in extracellular histamine levels. (2) Neither IL-3 nor IgE induced histamine production in the presence of the specific inhibitor of histidine decarboxylase (HDC), the histamine-forming enzyme. (3) Both the enzymatic activity and the mRNA expression of HDC were enhanced in response to IL-3 or IgE. Artificial aggregation or formation of IgE immune complexes augmented ther effect on histamine synthesis, indicating that the aggregated form is responsible for this biologic activity. Yet, it is apparently not mediated by Fc epsilon RI because their cross-linkage by dinitrophenyl bovine serum albumin after presensitization with IgE did not induce histamine production by hematopoietic progenitors. Among other aggregated isotypes tested, only IgG2a and, to a lesser extent, IgG1 had a consistent but lower effect, whereas IgM and IgA were completely inactive. The target cells of IL-3 and IgE in terms of histamine synthesis do not belong to mature bone marrow populations, especially mast cells. They copurify with hematopoietic progenitors in the low-density layers of a discontinuous Ficoll gradient where they represent around 5% of the cells, as determined by in situ hybridization. This percentage remained the same, regardless of whether the cells were stimulated by IgE or IL-3 alone or by a combination of both, suggesting a common responder cell. In accordance with this notion, histamine-producing cells could not be distinguished from each other on the basis of density, size and internal structure, or rhodamine (Rh) retention. Finally, the effect of IgE is not caused by the induction of IL-3 because anti-IL-3 antibodies did not abrogate the effect of IgE.

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Salachas, F., E. Schneider, FM Lemoine, B. Lebel, M. Daeron, S. Navarro, H. Ziltener, and M. Dy. "Aggregated IgE mimic interleukin-3-induced histamine synthesis by murine hematopoietic progenitors." Blood 84, no. 4 (August 15, 1994): 1098–107. http://dx.doi.org/10.1182/blood.v84.4.1098.bloodjournal8441098.

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Similar to interleukin-3 (IL-3), IgE acts on murine bone marrow cells by inducing histamine production. This effect does not result from degranulation of histamine-containing cells, but from histamine synthesis, as assessed by the following findings. (1) The histamine content of freshly isolated bone marrow cells is too low to account for the increase in extracellular histamine levels. (2) Neither IL-3 nor IgE induced histamine production in the presence of the specific inhibitor of histidine decarboxylase (HDC), the histamine-forming enzyme. (3) Both the enzymatic activity and the mRNA expression of HDC were enhanced in response to IL-3 or IgE. Artificial aggregation or formation of IgE immune complexes augmented ther effect on histamine synthesis, indicating that the aggregated form is responsible for this biologic activity. Yet, it is apparently not mediated by Fc epsilon RI because their cross-linkage by dinitrophenyl bovine serum albumin after presensitization with IgE did not induce histamine production by hematopoietic progenitors. Among other aggregated isotypes tested, only IgG2a and, to a lesser extent, IgG1 had a consistent but lower effect, whereas IgM and IgA were completely inactive. The target cells of IL-3 and IgE in terms of histamine synthesis do not belong to mature bone marrow populations, especially mast cells. They copurify with hematopoietic progenitors in the low-density layers of a discontinuous Ficoll gradient where they represent around 5% of the cells, as determined by in situ hybridization. This percentage remained the same, regardless of whether the cells were stimulated by IgE or IL-3 alone or by a combination of both, suggesting a common responder cell. In accordance with this notion, histamine-producing cells could not be distinguished from each other on the basis of density, size and internal structure, or rhodamine (Rh) retention. Finally, the effect of IgE is not caused by the induction of IL-3 because anti-IL-3 antibodies did not abrogate the effect of IgE.

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Van Oostdam, J. C., D. C. Walker, K. Knudson, P. Dirks, R. W. Dahlby, and J. C. Hogg. "Effect of breathing dry air on structure and function of airways." Journal of Applied Physiology 61, no. 1 (July 1, 1986): 312–17. http://dx.doi.org/10.1152/jappl.1986.61.1.312.

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We compared the effect of breathing dry air (0.70 mg H2O/l) with that of breathing room air (8.62 mg H2O/l) in guinea pigs anesthetized with urethane. The data showed that breathing dry air caused a reduction of extravascular water (EVW) in the trachea (P less than 0.01) but not the lung. Structural analysis showed that this water loss occurred from the loose connective tissue of the submucosa. Histamine dose response curves performed on the animals showed that breathing dry air caused an increase in the maximum response (delta max RL) (P less than 0.01) without changing either the dose required to produce 50% of the delta max RL or the ratio of delta max RL to this dose. We conclude that breathing dry air produces an acute reduction of EVW of the loose connective tissue of the airways and an increase in the maximum response to histamine.

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Schneider, E., RE Ploemacher, B. Nabarra, NH Brons, and M. Dy. "Mast cells and their committed precursors are not required for interleukin-3-induced histamine synthesis in murine bone marrow: characteristics of histamine-producing cells." Blood 81, no. 5 (March 1, 1993): 1161–69. http://dx.doi.org/10.1182/blood.v81.5.1161.1161.

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Abstract In the present study we investigate the nature of the murine bone marrow cell subset responsible for the marked increase in histamine synthesis induced by interleukin-3 (IL-3). Because mast cells, and eventually their committed precursors, represent a potential source of histamine in this context, we examined their possible participation in this biologic activity with particular attention. We provide evidence that neither of these populations respond to IL-3 in terms of histamine synthesis and that other differentiated end cells or stromal components of the bone marrow are also not involved in this phenomenon. Starting from these findings, we further characterized the immature hematopoietic compartment responsible for IL-3-induced histamine synthesis using fluorescence-activated cell sorter (FACS) sorting based on rhodamine retention or wheat germ agglutinin (WGA) affinity. These procedures have allowed us to ascribe the following features to histamine-producing cells: (1) They belong to a low-density, progenitor- enriched bone marrow subset containing cells of relatively important size and internal structure. (2) The highest histamine levels are generated by the rhodamine-bright fraction of this population, while the most primitive rhodamine-dull cells do not express this biologic activity. (3) Histamine-producing cells do not copurify with colony- forming units in spleen day 7 and day 12 in WGA-bright fractions. (4) Their enrichment is associated with increased frequencies of cells forming colonies in methylcellulose (CFU-C), suggesting the involvement of several progenitors with partially limited differentiation potential in this biologic activity.

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Schneider, E., RE Ploemacher, B. Nabarra, NH Brons, and M. Dy. "Mast cells and their committed precursors are not required for interleukin-3-induced histamine synthesis in murine bone marrow: characteristics of histamine-producing cells." Blood 81, no. 5 (March 1, 1993): 1161–69. http://dx.doi.org/10.1182/blood.v81.5.1161.bloodjournal8151161.

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In the present study we investigate the nature of the murine bone marrow cell subset responsible for the marked increase in histamine synthesis induced by interleukin-3 (IL-3). Because mast cells, and eventually their committed precursors, represent a potential source of histamine in this context, we examined their possible participation in this biologic activity with particular attention. We provide evidence that neither of these populations respond to IL-3 in terms of histamine synthesis and that other differentiated end cells or stromal components of the bone marrow are also not involved in this phenomenon. Starting from these findings, we further characterized the immature hematopoietic compartment responsible for IL-3-induced histamine synthesis using fluorescence-activated cell sorter (FACS) sorting based on rhodamine retention or wheat germ agglutinin (WGA) affinity. These procedures have allowed us to ascribe the following features to histamine-producing cells: (1) They belong to a low-density, progenitor- enriched bone marrow subset containing cells of relatively important size and internal structure. (2) The highest histamine levels are generated by the rhodamine-bright fraction of this population, while the most primitive rhodamine-dull cells do not express this biologic activity. (3) Histamine-producing cells do not copurify with colony- forming units in spleen day 7 and day 12 in WGA-bright fractions. (4) Their enrichment is associated with increased frequencies of cells forming colonies in methylcellulose (CFU-C), suggesting the involvement of several progenitors with partially limited differentiation potential in this biologic activity.

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FLEMING, John V., Francisca SÁNCHEZ-JIMÉNEZ, Aurelio A. MOYA-GARCÍA, Michael R. LANGLOIS, and Timothy C. WANG. "Mapping of catalytically important residues in the rat l-histidine decarboxylase enzyme using bioinformatic and site-directed mutagenesis approaches." Biochemical Journal 379, no. 2 (April 15, 2004): 253–61. http://dx.doi.org/10.1042/bj20031525.

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HDC (l-histidine decarboxylase), the enzyme responsible for the catalytic production of histamine from l-histidine, belongs to an evolutionarily conserved family of vitamin B6-dependent enzymes known as the group II decarboxylases. Yet despite the obvious importance of histamine, mammalian HDC enzymes remain poorly characterized at both the biochemical and structural levels. By comparison with the recently described crystal structure of the homologous enzyme l-DOPA decarboxylase, we have been able to identify a number of conserved domains and motifs that are important also for HDC catalysis. This includes residues that were proposed to mediate events within the active site, and HDC proteins carrying mutations in these residues were inactive when expressed in reticulocyte cell lysates reactions. Our studies also suggest that a significant change in quartenary structure occurs during catalysis. This involves a protease sensitive loop, and incubating recombinant HDC with an l-histidine substrate analogue altered enzyme structure so that the loop was no longer exposed for tryptic proteolysis. In total, 27 mutant proteins were used to test the proposed importance of 34 different amino acid residues. This is the most extensive mutagenesis study yet to identify catalytically important residues in a mammalian HDC protein sequence and it provides a number of novel insights into the mechanism of histamine biosynthesis.

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Gbahou, Florence, Ludwig Vincent, Marie Humbert-Claude, Joel Tardivel-Lacombe, Claude Chabret, and Jean-Michel Arrang. "Compared pharmacology of human histamine H3 and H4 receptors: structure-activity relationships of histamine derivatives." British Journal of Pharmacology 147, no. 7 (April 2006): 744–54. http://dx.doi.org/10.1038/sj.bjp.0706666.

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36

Liu, Chen, and Khalil A. Abboud. "Crystal structures of μ-oxalato-bis[azido(histamine)copper(II)] and μ-oxalato-bis[(dicyanamido)(histamine)copper(II)]." Acta Crystallographica Section E Crystallographic Communications 71, no. 11 (October 28, 2015): 1379–83. http://dx.doi.org/10.1107/s2056989015019908.

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The title compounds, μ-oxalato-κ4O1,O2:O1′,O2′-bis[[4-(2-aminoethyl)-1H-imidazole-κ2N3,N4](azido-κN1)copper(II)], [Cu2(C2O4)(N3)2(C5H9N3)2], (I), and μ-oxalato-κ4O1,O2:O1′,O2′-bis[[4-(2-aminoethyl)-1H-imidazole-κ2N3,N4](dicyanamido-κN1)copper(II)], [Cu2(C2O4)(C2N3)2(C5H9N3)2], (II), are two oxalate-bridged dinuclear copper complexes. Each CuIIion adopts a five-coordinate square-pyramidal coordination sphere where the basal N2O2plane is formed by two O atoms of the oxalate ligand and two N atoms of a bidentate chelating histamine molecule. The apical coordination site in compound (I) is occupied by a monodentate azide anion through one of its terminal N atoms. The apical coordination site in compound (II) is occupied by a monodentate dicyanamide anion through one of its terminal N atoms. The molecules in both structures are centrosymmetric. In the crystals of compounds (I) and (II), the dinuclear complexes are linked through N—H...Xand C—H...X(X= N, O) hydrogen bonds where the donors are provided by the histamine ligand and the acceptor atoms are provided by the azide, dicyanamide, and oxalate ligands. In compound (I), the coordinatively unsaturated copper ions interact with the histamine ligandviaa C—H...Cu interaction. The coordinatively unsaturated copper ions in compound (II) interactviaa weak N...Cu interaction with the dicyanamide ligand of a neighboring molecule. The side chain of the histamine ligand is disordered over three sets of sites in (II).

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Shimamura, T., M. Shiroishi, S. Weyand, H. Tsujimoto, G. Winter, V. Katritch, R. Abagyan, et al. "Structure of the human histamine H1 receptor with doxepin." Acta Crystallographica Section A Foundations of Crystallography 67, a1 (August 22, 2011): C185—C186. http://dx.doi.org/10.1107/s0108767311095377.

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Raczynska, Ewa D., Michal K. Cyranski, Malgorzata Darowska, and Tomasz Rudka. "ChemInform Abstract: Structure and Proton Transfer Reactions in Histamine." ChemInform 32, no. 46 (May 23, 2010): no. http://dx.doi.org/10.1002/chin.200146299.

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Birdsall, Nigel J. M. "Cloning and structure-function of the H2 histamine receptor." Trends in Pharmacological Sciences 12 (January 1991): 9–10. http://dx.doi.org/10.1016/0165-6147(91)90481-7.

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Chen, Peng, Meiqi Zhang, Wenbin Sun, Hongfeng Li, Lang Zhao, and Pengfei Yan. "Anion-dependent assembly of Dy complexes: structures and magnetic behaviors." CrystEngComm 17, no. 27 (2015): 5066–73. http://dx.doi.org/10.1039/c5ce00925a.

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The in situ reaction of 2-aldehyde-8-hydroxyquinoline, histamine and LnX₃·6H₂O (X⁻ = OAc⁻, NO₃⁻ and ClO₄⁻) affords three distinct species of eight lanthanide complexes.

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Zhang, Erkang, Yani Zhang, Zhuoyan Fan, Lei Cheng, Shiwen Han, and Huilian Che. "Apigenin Inhibits Histamine-Induced Cervical Cancer Tumor Growth by Regulating Estrogen Receptor Expression." Molecules 25, no. 8 (April 23, 2020): 1960. http://dx.doi.org/10.3390/molecules25081960.

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Apigenin is a natural flavone with anti-inflammatory and antioxidant properties and antitumor abilities against several types of cancers. Previous studies have found that the antitumor effects of apigenin may be due to its similar chemical structure to 17β-estradiol (E2), a main kind of estrogen in women. However, the precise mechanism underlying the antitumor effects of apigenin in cervical cancer remains unknown. On the other hand, there is increasing evidence that describes a histamine role in cancer cell proliferation. In this study, we examined whether apigenin can attenuate the effects of histamine on tumors by regulating the expression level of estrogen receptors (ERs) to inhibit cervical cancer growth. Our in vitro data indicates that apigenin inhibited cell proliferation in a dose-dependent manner in human cervical cancer cells (HeLa), while histamine shows the opposite effects. After that, the xenograft model was established to explore the antitumor effects of apigenin in vivo, the results show that apigenin inhibited cervical tumor growth by reversing the abnormal ER signal in tumor tissue which was caused by histamine. We also demonstrate that apigenin inhibited cell proliferation via suppressing the PI3K/Akt/mTOR signaling pathway. Collectively, our results suggest that apigenin may inhibit tumor growth through the ER-mediated PI3K/Akt/mTOR pathway and that it can also attenuate the effects of histamine on tumors.

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Zhang, Yu-Shi, Jia-Yin Han, Omer Iqbal, and Ai-Hua Liang. "Research Advances and Prospects on Mechanism of Sinomenin on Histamine Release and the Binding to Histamine Receptors." International Journal of Molecular Sciences 20, no. 1 (December 24, 2018): 70. http://dx.doi.org/10.3390/ijms20010070.

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Sinomenine (SIN) is widely used in China to treat a variety of rheumatic diseases (RA), and has various pharmacological effects such as anti-inflammatory, analgesic, and anti-tumor effects. However, due to the histamine release characteristics of SIN, its adverse reactions such as allergic reactions, gastrointestinal reactions, and circulatory systemic reactions have been drawing increasing attention. We present here a systematic review of the chemical structure, pharmacological effects, clinical application, and adverse reactions of SIN, a detailed discussion on the relationship between histamine/histamine receptor and mechanism of action of SIN. In addition, we simulated the binding of SIN to four histamine receptors by using a virtual molecular docking method and found that the bonding intensity between SIN and receptors varied in the order shown as follows: H1R > H2R ~ H3R > H4R. The docking results suggested that SIN might exhibit dual regulatory effects in many processes such as cyclooxygenase-2 (COX-2) expression, NF-κB pathway activation, and degranulation of mast cells to release histamine, thereby exhibiting pro-inflammatory (adverse reactions)/anti-inflammatory effects. This study provides a theoretical basis for the clinical treatment of inflammations seen such as in RA using SIN, and also suggests that SIN has great potential in the field of cancer treatment and will have very important social and economic significance.

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Skoutakis, Vasilios A. "Comparison of the Parenteral Histamine2-Receptor Antagonists." DICP 23, no. 10_suppl (October 1989): S17—S22. http://dx.doi.org/10.1177/1060028089023s1003.

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The chemical structure, pharmacokinetic properties, and drug–drug interaction profiles of the parenterally available histamine2 (H2)-receptor antagonists were compared. Famotidine is a guanidinothiazole derivative, ranitidine contains an aminomethylfuran ring, and cimetidine has an imidazole ring. Data from the literature indicate that because of its chemical structure famotidine has a much greater potency and affinity for the H2-receptor and a notable lack of drug–drug interactions when compared with ranitidine and cimetidine. As a result, famotidine should be considered the H2-receptor antagonist of choice for critically ill patients who require gastric-acid suppression and at the same time are being treated with other drugs that depend on the cytochrome P-450 mixed-function oxidase system for their metabolism and/or on renal tubular mechanisms for their excretion.

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Conrad, Marcus, Christian A. Söldner, Yinglong Miao, and Heinrich Sticht. "Agonist Binding and G Protein Coupling in Histamine H2 Receptor: A Molecular Dynamics Study." International Journal of Molecular Sciences 21, no. 18 (September 12, 2020): 6693. http://dx.doi.org/10.3390/ijms21186693.

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The histamine H2 receptor (H2R) plays an important role in the regulation of gastric acid secretion. Therefore, it is a main drug target for the treatment of gastroesophageal reflux or peptic ulcer disease. However, there is as of yet no 3D-structural information available hampering a mechanistic understanding of H2R. Therefore, we created a model of the histamine-H2R-Gs complex based on the structure of the ternary complex of the β2-adrenoceptor and investigated the conformational stability of this active GPCR conformation. Since the physiologically relevant motions with respect to ligand binding and conformational changes of GPCRs can only partly be assessed on the timescale of conventional MD (cMD) simulations, we also applied metadynamics and Gaussian accelerated molecular dynamics (GaMD) simulations. A multiple walker metadynamics simulation in combination with cMD was applied for the determination of the histamine binding mode. The preferential binding pose detected is in good agreement with previous data from site directed mutagenesis and provides a basis for rational ligand design. Inspection of the H2R-Gs interface reveals a network of polar interactions that may contribute to H2R coupling selectivity. The cMD and GaMD simulations demonstrate that the active conformation is retained on a μs-timescale in the ternary histamine-H2R-Gs complex and in a truncated complex that contains only Gs helix α5 instead of the entire G protein. In contrast, histamine alone is unable to stabilize the active conformation, which is in line with previous studies of other GPCRs.

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Janssen, Daniel, Christian Derst, Jean-Michel Rigo, and Emmy Van Kerkhove. "Cys-Loop Ligand-Gated Chloride Channels in Dorsal Unpaired Median Neurons of Locusta migratoria." Journal of Neurophysiology 103, no. 5 (May 2010): 2587–98. http://dx.doi.org/10.1152/jn.00466.2009.

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In insects, inhibitory neurotransmission is generally associated with members of the cys-loop ligand-gated anion channels, such as the glutamate-gated chloride channel (GluCl), the GABA-gated chloride channels (GABACl), and the histamine-gated chloride channels (HisCl). These ionotropic receptors are considered established target sites for the development of insecticides, and therefore it is necessary to obtain a better insight in their distribution, structure, and functional properties. Here, by combining electrophysiology and molecular biology techniques, we identified and characterized GluCl, GABACl, and HisCl in dorsal unpaired median (DUM) neurons of Locust migratoria. In whole cell patch-clamp recordings, application of glutamate, GABA, or histamine induced rapidly activating ionic currents. GluCls were sensitive to ibotenic acid and blocked by picrotoxin and fipronil. The pharmacological profile of the L. migratoria GABACl fitted neither the vertebrate GABAA nor GABAC receptor and was similar to the properties of the cloned Drosophila melanogaster GABA receptor subunit (Rdl). The expression of Rdl-like subunit-containing GABA receptors was shown at the molecular level using RT-PCR. Sequencing analysis indicated that the orthologous GABACl of D. melanogaster CG10357-A is expressed in DUM neurons of L. migratoria. Histamine-induced currents exhibited a fast onset and desensitized completely on continuous application of histamine. In conclusion, within the DUM neurons of L. migratoria, we identified three different cys-loop ligand-gated anion channels that use GABA, glutamate, or histamine as their neurotransmitter.

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Istyastono, Enade P., Albert J. Kooistra, Henry F. Vischer, Martien Kuijer, Luc Roumen, Saskia Nijmeijer, Rogier A. Smits, Iwan J. P. de Esch, Rob Leurs, and Chris de Graaf. "Structure-based virtual screening for fragment-like ligands of the G protein-coupled histamine H4 receptor." MedChemComm 6, no. 6 (2015): 1003–17. http://dx.doi.org/10.1039/c5md00022j.

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Structure-based virtual screening using H₁R- and β₂R-based histamine H₄R homology models identified 9 fragments with an affinity ranging from 0.14 to 6.3 μm for H₄R.

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Bannister, C., K. Burns, K. Prout, D. J. Watkin, D. G. Cooper, G. J. Durant, C. R. Ganellin, R. J. Ife, and G. S. Sach. "Structures of histamine H1-receptor antagonists derived from the cimetidine group of histamine H2-receptor antagonists." Acta Crystallographica Section B Structural Science 50, no. 2 (April 1, 1994): 221–43. http://dx.doi.org/10.1107/s0108768193010407.

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URATANI, Yoshihiko, Keiko TAKIGUCHI-HAYASHI, Nobuhiko MIYASAKA, Michio SATO, Ming-hao JIN, and Yasuyoshi ARIMATSU. "Latexin, a carboxypeptidase A inhibitor, is expressed in rat peritoneal mast cells and is associated with granular structures distinct from secretory granules and lysosomes." Biochemical Journal 346, no. 3 (March 7, 2000): 817–26. http://dx.doi.org/10.1042/bj3460817.

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Latexin, a protein possessing inhibitory activity against rat carboxypeptidase A1 (CPA1) and CPA2, is expressed in a neuronal subset in the cerebral cortex and cells in other neural and non-neural tissues of rat. Although latexin also inhibits mast-cell CPA (MCCPA), the expression of latexin in rat mast cells has not previously been confirmed. In the present study we examined the expression and subcellular localization of latexin in rat peritoneal mast cells. Western blot and reverse-transcriptase-mediated PCR analyses showed that latexin was contained and expressed in the rat peritoneal mast cells. Immunocytochemically, latexin immunofluorescence was localized on granular structures distinct from MCCPA-, histamine- or cathepsin D-immunopositive granules. Immunoelectron microscopy revealed that latexin was associated with a minority population of granules. The latexin-associated granules were separated from MCCPA- or histamine-containing granules on a self-generating density gradient of polyvinylpyrrolidone-coated silica-gel particles (Percoll). Treatments with high ionic strength and heparinase released latexin from the granules, suggesting that latexin is non-covalently associated with a heparin-like component of the granules. MCCPA and histamine were released from the mast cells after non-immunological and immunological stimulation with compound 48/80, A23187 and anti-IgE antibody, whereas latexin was not released. These results show that latexin is synthesized in rat peritoneal mast cells and suggest that it is associated with a unique type of intracellular granules distinct from MCCPA- and histamine-containing secretory granules and lysosomes.

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Fujimoto, Katsumi, Kazuichi Sakamoto, Seiji Ito, Satoshi Ogino, and Hiroyuki Fukui. "ANALYSIS OF PRIMARY STRUCTURE OF HUMAN HISTAMINE H1 RECEPTOR mRNA." Japanese Journal of Pharmacology 71 (1996): 70. http://dx.doi.org/10.1016/s0021-5198(19)36520-5.

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Shimamura, Tatsuro, Mitsunori Shiroishi, Simone Weyand, Hirokazu Tsujimoto, Graeme Winter, Vsevolod Katritch, Ruben Abagyan, et al. "Structure of the human histamine H1 receptor complex with doxepin." Nature 475, no. 7354 (June 22, 2011): 65–70. http://dx.doi.org/10.1038/nature10236.

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Journal articles on the topic 'Structure of histamines'

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